One-liner#

Chronic insomnia management prioritizes CBT-I as first-line therapy (more effective than medications long-term), with pharmacotherapy reserved for short-term use or CBT-I adjunct; avoid chronic hypnotic use due to dependence, tolerance, and cognitive effects, especially in elderly.

Quick nav#

• Definition and epidemiology
• Pathophysiology
• Clinical presentation
• Diagnostic workup
• Treatment
• Patient education
• Prognosis and monitoring
• Special populations
• When to refer
• Smartphrase snippets
• Related pages

Definition and epidemiology#

Diagnostic criteria#

DSM-5/ICSD-3 criteria for Chronic Insomnia Disorder:

A. Predominant complaint of dissatisfaction with sleep quantity or quality, with ≥1 of:

1. Difficulty initiating sleep (sleep-onset insomnia): >30 minutes to fall asleep
2. Difficulty maintaining sleep (sleep-maintenance insomnia): frequent awakenings or difficulty returning to sleep
3. Early morning awakening with inability to return to sleep

B. Sleep disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning

C. Sleep difficulty occurs ≥3 nights per week

D. Sleep difficulty is present for ≥3 months

E. Sleep difficulty occurs despite adequate opportunity for sleep

F. Not better explained by another sleep disorder (OSA, RLS, circadian rhythm disorder)

G. Not attributable to substance use or medication effects

H. Coexisting mental disorders and medical conditions do not adequately explain the insomnia

Severity classification by Insomnia Severity Index (ISI):

Key distinctions:

• Acute insomnia: <3 months duration; often resolves with stressor removal
• Chronic insomnia: ≥3 months; requires active treatment
• Comorbid insomnia: occurs with psychiatric or medical condition but warrants independent treatment
• Short sleep duration phenotype: chronic insomnia with objective short sleep (<6 hours on PSG); associated with worse health outcomes

Epidemiology#

Chronic insomnia affects 10-15% of adults; insomnia symptoms (without full criteria) affect 30-35%. Female:male ratio is 1.4:1. Prevalence increases with age, peaking after age 65. Insomnia is the most common sleep complaint in primary care.

Risk factors:

• Female sex
• Age >65 years
• Family history (35-40% heritability)
• Psychiatric disorders (depression, anxiety, PTSD)
• Chronic medical conditions (chronic pain, COPD, heart failure)
• Shift work or irregular schedules
• Low socioeconomic status
• Hyperarousal personality traits (perfectionism, rumination)

Comorbidity rates:

• Depression: 40-60% (bidirectional relationship)
• Anxiety disorders: 30-50%
• Chronic pain: 50-70%
• Cardiovascular disease: increased risk (OR 1.4-1.5)
• Hypertension: 20-30% increased risk
• Type 2 diabetes: increased risk
• Obesity: bidirectional relationship

Pathophysiology#

Mechanism (clinical understanding)#

Chronic insomnia is best understood through the 3P model (Spielman model), which explains why acute insomnia becomes chronic and why behavioral interventions are effective.

Predisposing factors (trait vulnerability):

• Genetic predisposition (heritability ~35-40%)
• Hyperarousal trait: tendency toward heightened physiological and cognitive arousal
• Personality factors: perfectionism, rumination, anxiety sensitivity
• Female sex, older age

Precipitating factors (trigger):

• Acute stressors: job loss, divorce, illness, bereavement
• Medical events: hospitalization, surgery, new diagnosis
• Environmental changes: new baby, travel, shift work
• Substance use or withdrawal

Perpetuating factors (what maintains chronic insomnia):

• Maladaptive sleep behaviors: excessive time in bed, irregular schedule, napping
• Conditioned arousal: bed becomes associated with wakefulness and frustration
• Dysfunctional beliefs: catastrophizing about sleep consequences
• Safety behaviors: clock-watching, trying too hard to sleep

Hyperarousal model: The core pathophysiology of chronic insomnia is 24-hour hyperarousal—not just at night. Patients with chronic insomnia show:

• Elevated cortisol levels throughout the day
• Increased metabolic rate (higher body temperature, heart rate)
• Heightened sympathetic nervous system activity
• Increased high-frequency EEG activity during sleep (brain doesn’t fully “turn off”)
• Elevated inflammatory markers (IL-6, TNF-α)

This explains why patients feel “tired but wired”—they’re exhausted but can’t relax enough to sleep.

Conditioned arousal: Through classical conditioning, the bed and bedroom become associated with wakefulness rather than sleep. Lying in bed awake, frustrated, and anxious creates a learned association: bed = arousal. This is why patients often sleep better in novel environments (hotels, sleep labs) and why stimulus control therapy works.

Sleep state misperception: Many patients with chronic insomnia underestimate their actual sleep time. Objective polysomnography often shows more sleep than patients report. This isn’t “faking”—it reflects altered sleep perception due to hyperarousal (light, fragmented sleep feels like wakefulness).

Neurobiological mechanisms:

• GABA system: reduced GABAergic inhibition in insomnia; explains why GABA-enhancing drugs (benzodiazepines, Z-drugs) provide short-term relief
• Orexin/hypocretin system: promotes wakefulness; overactive in insomnia; target of newer medications (suvorexant, lemborexant)
• Melatonin: may be phase-shifted or reduced; explains modest benefit of exogenous melatonin

How to explain to patients#

Insomnia isn’t just about not sleeping—it’s about your brain being stuck in “alert mode” even when you’re exhausted.

Think of your brain like a car engine. Normally, when you go to bed, the engine idles down and eventually turns off. But with insomnia, the engine keeps revving even when you’re trying to rest. You feel tired, but your brain won’t shut down.

This happens because of a cycle that develops over time. When you can’t sleep, you start worrying about sleep. You spend more time in bed trying to catch up. You start associating your bed with frustration and wakefulness instead of rest. Your brain learns: “bed = stay alert.” This makes the problem worse.

The good news is that this cycle can be broken. The most effective treatment isn’t a pill—it’s retraining your brain to associate bed with sleep again. This is called CBT-I (cognitive behavioral therapy for insomnia). It works by:

• Limiting time in bed so you’re actually sleepy when you lie down
• Getting out of bed when you can’t sleep (breaking the bed-wakefulness association)
• Keeping a consistent schedule to reset your internal clock
• Changing unhelpful thoughts about sleep

Medications can help in the short term, but they don’t fix the underlying problem. They’re like putting a bandage on a wound without cleaning it—it might look better temporarily, but the real healing comes from addressing the root cause.

Clinical presentation#

Characteristic symptoms#

Sleep complaints (at least one required):

• Sleep-onset insomnia: difficulty falling asleep (>30 minutes)
• Sleep-maintenance insomnia: frequent awakenings (>30 minutes awake during night)
• Early morning awakening: waking 2+ hours before desired time, unable to return to sleep
• Non-restorative sleep: sleep feels unrefreshing despite adequate duration

Daytime consequences:

• Fatigue: “exhausted,” “no energy” (distinct from sleepiness)
• Cognitive impairment: difficulty concentrating, memory problems, “brain fog”
• Mood disturbance: irritability, low mood, emotional reactivity
• Reduced motivation and initiative
• Impaired work/school performance
• Increased errors and accidents
• Social/relationship difficulties

Hyperarousal symptoms:

• Racing thoughts at bedtime
• Difficulty “turning off” the mind
• Physical tension (muscle tension, jaw clenching)
• Heightened awareness of environment (noises, light)
• Anxiety about sleep itself (“sleep anxiety”)
• Clock-watching behavior

Compensatory behaviors (perpetuating factors):

• Spending excessive time in bed
• Irregular sleep schedule
• Daytime napping
• Using alcohol as a sleep aid
• Excessive caffeine to combat daytime fatigue
• Avoiding activities due to fatigue

Physical exam findings#

General appearance:

• May appear fatigued (dark circles, yawning)
• Usually not overtly sleepy (hyperarousal keeps them alert)
• May appear tense, anxious

Vital signs:

• Usually normal
• May have mildly elevated resting heart rate (hyperarousal)
• Blood pressure may be mildly elevated

Physical exam (to rule out contributing conditions):

• Thyroid: goiter, nodules (hyperthyroidism causes insomnia)
• Airway: Mallampati score, neck circumference (OSA screening)
• Cardiovascular: signs of heart failure (orthopnea, edema)
• Neurologic: restless legs (observe for movements), neuropathy
• Musculoskeletal: pain sources

Mental status exam:

• Appearance: fatigued but alert
• Mood: may report “tired,” “frustrated,” “anxious”
• Affect: may be irritable, anxious
• Thought content: worry about sleep, catastrophizing about consequences
• Cognition: may have subjective concentration difficulties
• Screen for depression (PHQ-9) and anxiety (GAD-7)

Red flags#

Symptoms suggesting alternative sleep disorder:

• Loud snoring, witnessed apneas, gasping → obstructive sleep apnea
• Urge to move legs, worse at rest/night, relieved by movement → restless legs syndrome
• Excessive daytime sleepiness (falling asleep unintentionally) → OSA, narcolepsy
• Abnormal behaviors during sleep (walking, eating, violence) → parasomnia
• Inability to sleep at desired time but normal sleep at other times → circadian rhythm disorder

Psychiatric emergencies:

• Suicidal ideation (insomnia is a risk factor for suicide)
• Mania/hypomania: decreased NEED for sleep (not insomnia); do NOT give hypnotics
• Severe depression with psychomotor retardation

Medical red flags:

• New-onset insomnia with weight loss, night sweats → malignancy workup
• Insomnia with palpitations, tremor, heat intolerance → hyperthyroidism
• Insomnia with severe pain → inadequate pain control

Diagnostic workup#

Initial evaluation#

Sleep diary (essential—have patient complete for 1-2 weeks):

• Bedtime and wake time
• Estimated time to fall asleep (sleep onset latency)
• Number and duration of nighttime awakenings
• Final wake time and time out of bed
• Estimated total sleep time
• Sleep quality rating (1-10)
• Daytime naps (time and duration)
• Caffeine, alcohol, medication use
• Notes on factors affecting sleep

Insomnia Severity Index (ISI)—administer at baseline and follow-up:

• 7 items scored 0-4; total 0-28
• Validated for screening and monitoring treatment response
• Clinically significant change: ≥6-point reduction

Screen for comorbid conditions:

Baseline labs (only if clinical suspicion for medical cause):

Most chronic insomnia is diagnosed clinically. Extensive labs are NOT needed.

Confirmatory testing#

Polysomnography (sleep study)—NOT routinely indicated for insomnia:

Actigraphy (wrist-worn activity monitor):

• Useful for assessing sleep-wake patterns over 1-2 weeks
• Helpful for circadian rhythm disorders
• Can validate sleep diary data
• Not routinely needed for typical insomnia

When to refer for specialist workup#

• Suspected obstructive sleep apnea → sleep medicine for PSG
• Suspected narcolepsy or hypersomnia → sleep medicine
• Suspected parasomnia (sleepwalking, REM behavior disorder) → sleep medicine
• Treatment-refractory insomnia (failed CBT-I + 2 medication trials) → sleep medicine or behavioral sleep medicine
• Complex circadian rhythm disorders → sleep medicine
• Insomnia with severe psychiatric comorbidity → psychiatry

What NOT to order#

• Polysomnography for typical chronic insomnia: Clinical diagnosis; PSG doesn’t change management
• Extensive blood work: Insomnia is rarely caused by occult medical conditions
• Brain imaging: Not indicated unless focal neurologic findings
• Genetic testing: No clinical utility
• Multiple sleep latency test (MSLT): Only for suspected narcolepsy, not insomnia

Treatment#

Goals of therapy#

Primary goals:

• Remission: ISI <8 (no clinically significant insomnia)
• Improved sleep efficiency: >85% (time asleep / time in bed)
• Reduced sleep onset latency: <30 minutes
• Reduced wake after sleep onset: <30 minutes
• Improved daytime functioning
• Discontinuation of hypnotic medications (if applicable)

Treatment targets:

Important: Total sleep time is NOT the primary target. Some patients have lower sleep needs. Focus on sleep quality and daytime functioning.

Non-pharmacologic management#

CBT-I (Cognitive Behavioral Therapy for Insomnia)—FIRST-LINE TREATMENT

CBT-I is more effective than medications for chronic insomnia and should be offered to ALL patients. Effects persist after treatment ends (unlike medications).

Evidence:

• NNT = 2-3 for clinically significant improvement
• 70-80% of patients improve with CBT-I
• Effects maintained at 1-year follow-up
• Reduces hypnotic use
• Effective even with comorbid depression, anxiety, chronic pain

CBT-I components:

Sleep restriction protocol (core component):

1. Calculate average total sleep time from sleep diary (e.g., 5.5 hours)
2. Set time in bed = total sleep time (minimum 5 hours)
3. Set fixed wake time (e.g., 6:00 AM)
4. Calculate bedtime (e.g., 12:30 AM for 5.5 hours)
5. When sleep efficiency >85% for 5 days, add 15-30 minutes to time in bed
6. Repeat until optimal sleep duration achieved

Stimulus control rules:

• Go to bed only when sleepy
• Use bed only for sleep and sex (no TV, phone, reading, worrying)
• If unable to sleep within ~20 minutes, get up and go to another room
• Do something relaxing (dim light, no screens) until sleepy, then return to bed
• Repeat as needed
• Wake at the same time every day regardless of sleep quality
• No daytime napping

CBT-I delivery options:

Recommend CBT-I for:

• All patients with chronic insomnia (first-line)
• Patients wanting to avoid or discontinue medications
• Patients with comorbid conditions (depression, anxiety, chronic pain)
• Elderly patients (avoids medication risks)
• Pregnant/breastfeeding patients

Sleep hygiene education (adjunct, not sufficient alone):

• Consistent sleep/wake times 7 days/week (most important)
• Avoid caffeine after noon (half-life 5-6 hours)
• Avoid alcohol within 3 hours of bedtime (disrupts sleep architecture)
• Avoid nicotine near bedtime (stimulant)
• Regular exercise (but not within 3-4 hours of bedtime)
• Optimize sleep environment: dark, cool (65-68°F), quiet
• Avoid screens 30-60 minutes before bed (blue light suppresses melatonin)
• Avoid clock-watching (turn clock away from bed)

Sleep hygiene alone is NOT effective for chronic insomnia. It’s a necessary foundation but insufficient without CBT-I components.

Pharmacologic management#

Principles of medication use in chronic insomnia:

• Medications are SECOND-LINE to CBT-I
• Use for shortest duration possible (2-4 weeks for most hypnotics)
• Set expectations for discontinuation from the start
• Combine with CBT-I when possible (improves long-term outcomes)
• Avoid in elderly if possible (falls, cognitive impairment)
• Monitor for dependence, tolerance, and adverse effects

First-line medications (if pharmacotherapy needed):

Second-line medications (short-term use only):

Orexin receptor antagonists (newer option):

Medications to AVOID for chronic insomnia:

• Benzodiazepines (temazepam, triazolam, etc.): High dependence potential; tolerance; rebound insomnia; falls; cognitive impairment; Beers list
• Diphenhydramine (Benadryl, PM products): Anticholinergic effects; rapid tolerance; next-day sedation; cognitive impairment; Beers list
• Hydroxyzine (long-term): Anticholinergic; tolerance; not effective long-term
• Zolpidem (long-term): Dependence; complex sleep behaviors; falls; cognitive effects
• Alcohol: Disrupts sleep architecture; dependence; rebound insomnia
• Cannabis: Tolerance develops; withdrawal insomnia; impairs sleep quality

Medication selection by clinical scenario:

• First-line if medication needed: trazodone 25-50 mg or melatonin 1-3 mg
• Sleep-onset insomnia: melatonin, zaleplon, or zolpidem (short-term)
• Sleep-maintenance insomnia: doxepin, zolpidem CR, or suvorexant
• Comorbid depression: trazodone (add to SSRI) or mirtazapine
• Comorbid anxiety: trazodone or hydroxyzine (short-term)
• Elderly: doxepin 3 mg or low-dose trazodone; AVOID Z-drugs and benzos
• Substance use history: trazodone, doxepin, or melatonin (no abuse potential)
• Pregnancy: CBT-I first-line; avoid all hypnotics if possible

Patient counseling points#

When recommending CBT-I:

• “The most effective treatment for chronic insomnia isn’t a pill—it’s a specific type of therapy called CBT-I. It works by retraining your brain to sleep.”
• “CBT-I takes some effort and may feel counterintuitive at first. You’ll actually spend less time in bed initially. But it works better than medications and the effects last.”
• “You may feel more tired for the first 1-2 weeks as we restrict your time in bed. This is temporary and necessary to build up your sleep drive.”
• “I’m going to refer you to a sleep specialist / recommend this app / give you this workbook to guide you through CBT-I.”

When starting medication:

• “This medication is meant to be a short-term bridge while we work on the underlying problem. It’s not a long-term solution.”
• “Sleep medications can become less effective over time and can be hard to stop. That’s why we’ll plan to taper off within a few weeks.”
• “Don’t drink alcohol while taking this—it increases sedation and can be dangerous.”
• “Don’t drive or operate machinery until you know how this affects you. Some people have next-day drowsiness.”
• “Take it only when you have 7-8 hours available for sleep. Don’t take it if you need to wake up earlier.”

About Z-drugs specifically:

• “In rare cases, people do things while asleep on this medication—like eating, walking, or even driving—and don’t remember. If this happens, stop the medication and call us.”
• “This medication works best when used occasionally, not every night. Using it every night leads to tolerance.”

Monitoring and follow-up#

Initial treatment phase:

Maintenance phase:

• Every 1-3 months until stable
• Then every 6-12 months or as needed
• ISI at each visit
• Reinforce CBT-I principles
• Address relapse early

What to monitor:

Patient education#

What is this condition?#

Chronic insomnia is a sleep disorder where you have trouble falling asleep, staying asleep, or waking up too early—and it happens at least 3 nights a week for 3 months or more. It’s not just an occasional bad night; it’s a pattern that affects your daily life.

Insomnia is very common—about 1 in 10 adults has chronic insomnia. It’s more common in women and tends to increase with age.

Chronic insomnia isn’t just about not getting enough sleep. It’s about your brain being stuck in “alert mode.” Even when you’re exhausted, your brain won’t fully relax. This is why you might feel “tired but wired.”

The good news is that chronic insomnia is very treatable. The most effective treatment is a specific type of therapy called CBT-I (cognitive behavioral therapy for insomnia), which retrains your brain to sleep. It works better than sleeping pills and doesn’t have side effects.

What you can do#

Follow a consistent sleep schedule. Go to bed and wake up at the same time every day—even on weekends. This is the single most important thing you can do.

Use your bed only for sleep and sex. Don’t watch TV, scroll your phone, work, or worry in bed. If you can’t sleep after about 20 minutes, get up and do something relaxing in dim light until you feel sleepy.

Limit caffeine, especially after noon. Caffeine stays in your system for 5-6 hours. Even if you think it doesn’t affect you, it may be disrupting your sleep.

Avoid alcohol before bed. While alcohol might help you fall asleep, it disrupts your sleep later in the night and makes insomnia worse overall.

Create a relaxing bedtime routine. Dim the lights, avoid screens, and do something calming for 30-60 minutes before bed.

Don’t try to “catch up” on sleep. Sleeping in or napping makes insomnia worse by reducing your sleep drive at night.

Consider CBT-I. Ask your doctor about cognitive behavioral therapy for insomnia. It’s the most effective treatment and can be done with a therapist, online, or through apps.

When to seek care#

Call your doctor’s office if:

• Your insomnia is getting worse despite following sleep hygiene recommendations
• You’re having side effects from sleep medication
• You’re using sleep medication more often than prescribed
• You’re using alcohol or other substances to help you sleep
• Your insomnia is affecting your work, relationships, or safety

Seek urgent care if:

• You’re having thoughts of hurting yourself (insomnia increases suicide risk)
• You’re so sleep-deprived that you’re having trouble functioning safely (driving, working)
• You’re experiencing unusual behaviors during sleep (sleepwalking, sleep eating)

Questions to ask your doctor#

• What is my ISI score, and what does it mean?
• Should I try CBT-I? How do I access it?
• Do I need a sleep study?
• If I need medication, how long should I take it?
• How do I safely stop taking sleep medication?
• Could my insomnia be caused by another condition like sleep apnea or restless legs?
• Are any of my current medications affecting my sleep?
• When should I come back for follow-up?

Prognosis and monitoring#

Expected course#

With CBT-I treatment:

• 70-80% of patients show significant improvement
• Effects are durable—maintained at 1-year follow-up
• Many patients achieve remission (ISI <8)
• Improvement typically seen within 4-8 weeks
• Some patients need “booster” sessions for relapse

With medication alone:

• Short-term improvement in most patients
• Tolerance develops with nightly use (weeks to months)
• Relapse common when medication stopped
• Rebound insomnia with discontinuation
• Long-term use associated with adverse effects

Without treatment:

• Chronic insomnia rarely resolves spontaneously
• Tends to wax and wane but persists
• Associated with increased risk of depression, anxiety
• Associated with cardiovascular disease, diabetes
• Impaired quality of life and functioning

Factors predicting better outcome:

• Engagement with CBT-I
• Absence of severe psychiatric comorbidity
• Shorter duration of insomnia
• No chronic hypnotic use
• Good social support
• Motivation to change sleep behaviors

Factors predicting poorer outcome:

• Long-standing chronic hypnotic use
• Severe comorbid depression or anxiety
• Chronic pain
• Unrealistic sleep expectations
• Poor adherence to behavioral interventions

Monitoring parameters#

Complications to watch for#

Treatment-related (medications):

• Dependence and tolerance (especially Z-drugs, benzodiazepines)
• Next-day sedation and impaired driving
• Complex sleep behaviors (sleepwalking, sleep eating, sleep driving)
• Falls (especially elderly)
• Cognitive impairment (especially elderly, with chronic use)
• Rebound insomnia with discontinuation

Disease-related:

• Depression (insomnia is both a risk factor and symptom)
• Anxiety disorders
• Substance use (self-medication with alcohol, cannabis)
• Cardiovascular disease (chronic sleep deprivation)
• Impaired immune function
• Accidents (drowsy driving, workplace errors)
• Reduced quality of life

Special populations#

Elderly/geriatric#

Presentation differences:

• Sleep architecture changes with age (less deep sleep, more awakenings)
• Earlier bedtime and wake time (advanced sleep phase)
• May have unrealistic expectations (expecting 8 hours when 6-7 is normal)
• Higher rates of comorbid conditions affecting sleep
• More likely to be on medications that disrupt sleep

Treatment considerations:

• CBT-I is STRONGLY preferred (no fall risk, no cognitive effects)
• If medication needed: doxepin 3 mg or low-dose trazodone 25 mg
• AVOID (Beers criteria):
  • Benzodiazepines (falls, cognitive impairment, paradoxical agitation)
  • Z-drugs (falls, complex sleep behaviors, cognitive effects)
  • Diphenhydramine (anticholinergic, cognitive impairment)
  • First-generation antihistamines
• Start at lowest dose; titrate slowly
• Address nocturia, pain, and other contributors
• Screen for depression (often presents as insomnia in elderly)

Counseling:

• “Sleep needs decrease somewhat with age. Six to seven hours may be normal for you.”
• “Sleeping pills are particularly risky as we get older—they increase fall risk and can affect memory.”
• “The behavioral approach (CBT-I) is safer and more effective for you.”

Chronic kidney disease#

Considerations:

• High prevalence of sleep disorders in CKD (50-80%)
• Restless legs syndrome common (check ferritin)
• Sleep apnea common
• Uremia can cause sleep disruption
• Many hypnotics require dose adjustment

Medication adjustments:

Pregnancy and breastfeeding#

First-line: CBT-I

• Safe and effective
• No medication exposure to fetus/infant
• Should be offered to all pregnant patients with insomnia

If medication needed:

• Avoid all hypnotics in first trimester if possible
• Limited safety data for most sleep medications
• Diphenhydramine: occasionally used; limited data; avoid near delivery (neonatal effects)
• Doxylamine: used for nausea; some use for sleep; limited data
• Melatonin: insufficient safety data; avoid
• Z-drugs: limited data; potential risks; avoid
• Benzodiazepines: avoid (neonatal withdrawal, floppy infant syndrome)

Breastfeeding:

• CBT-I preferred
• Trazodone: low levels in breast milk; generally considered acceptable
• Z-drugs: excreted in breast milk; avoid or pump and dump

Refer to MFM or psychiatry for complex cases.

Comorbid psychiatric conditions#

Depression:

• Treat both conditions; they perpetuate each other
• CBT-I effective even with comorbid depression
• Sedating antidepressants can help both (mirtazapine, trazodone)
• Avoid activating antidepressants at bedtime (fluoxetine, bupropion)

Anxiety:

• CBT-I addresses anxiety-insomnia cycle
• SSRI/SNRI for anxiety may initially worsen insomnia (start low)
• Avoid benzodiazepines for sleep (dependence, doesn’t address underlying issue)
• Hydroxyzine can be used short-term

PTSD:

• Nightmares and hypervigilance disrupt sleep
• Prazosin for trauma-related nightmares
• CBT-I can be adapted for PTSD
• Refer to trauma-focused therapy

Bipolar disorder:

• Sleep disruption can trigger mood episodes
• Insomnia may herald mania
• Do NOT give hypnotics if mania suspected
• Quetiapine often used (mood stabilizer + sedating)
• Coordinate with psychiatry

Other populations#

Substance use disorders:

• Avoid medications with abuse potential (Z-drugs, benzodiazepines)
• Alcohol withdrawal causes severe insomnia
• Cannabis withdrawal causes insomnia
• Stimulant use disrupts sleep
• CBT-I is first-line (no abuse potential)
• If medication needed: trazodone, doxepin, or melatonin
• Address underlying substance use
• Expect sleep to improve as sobriety continues (may take weeks to months)

Polypharmacy considerations:

• Review all medications for sleep-disrupting effects (stimulants, diuretics, steroids, beta-blockers)
• Drug interactions: Z-drugs potentiated by CYP3A4 inhibitors; trazodone levels increased by CYP3A4 inhibitors
• Multiple sedating medications increase fall risk and cognitive impairment
• Simplify regimen when possible; avoid adding hypnotics to patients already on sedating medications

Shift workers:

• Circadian rhythm disruption is primary issue
• CBT-I principles still apply but timing adjusted
• Melatonin may help with circadian realignment
• Light therapy can help shift circadian rhythm
• Consider sleep medicine referral for complex cases

When to refer#

Specialist referral criteria#

Refer to behavioral sleep medicine / sleep psychologist:

• Patient interested in CBT-I but no local access
• Complex insomnia not responding to self-directed CBT-I
• Significant psychiatric comorbidity complicating treatment

Refer to sleep medicine:

• Suspected obstructive sleep apnea (STOP-BANG ≥3)
• Suspected other sleep disorder (narcolepsy, parasomnia, circadian rhythm disorder)
• Treatment-refractory insomnia (failed CBT-I + 2 medication trials)
• Need for polysomnography
• Complex hypnotic taper (long-term benzodiazepine use)

Refer to psychiatry:

• Severe comorbid depression or anxiety not responding to treatment
• Suspected bipolar disorder
• Suicidal ideation
• Complex medication management

Urgency levels#

Smartphrase snippets#

Stable/controlled chronic insomnia: Chronic insomnia, stable on current regimen with ISI [score] improved from baseline. Patient adherent to CBT-I principles including consistent sleep/wake times and stimulus control. Continue current approach; reinforce sleep hygiene; follow-up in [timeframe].

New diagnosis/initiating treatment: Chronic insomnia disorder meeting DSM-5 criteria with ISI [score] indicating [moderate/severe] insomnia; PHQ-9 [score], GAD-7 [score]; STOP-BANG [score] not concerning for OSA. Discussed CBT-I as first-line treatment—more effective than medications long-term. [Referred to behavioral sleep medicine / recommended Somryst app / provided CBT-I workbook]; sleep diary provided; follow-up in 2-4 weeks.

Tapering hypnotic medication: Chronic insomnia on [medication] for [duration]; discussed risks of long-term hypnotic use including dependence and cognitive effects. Plan: reduce dose by 25% every [1-2 weeks] with concurrent CBT-I to support taper. Expect temporary rebound insomnia which will improve; follow-up in [2-4 weeks].

Related pages#

• Insomnia (complaint) — symptom-based approach to insomnia evaluation and initial management
• Obstructive Sleep Apnea (problem) — OSA often coexists with or mimics insomnia
• Major Depressive Disorder (problem) — depression and insomnia are bidirectionally related
• Generalized Anxiety Disorder (problem) — anxiety commonly causes sleep-onset insomnia
• Depression (complaint) — insomnia as presenting symptom of depression
• Anxiety (complaint) — insomnia as presenting symptom of anxiety